Faculty Bio

Research Interests

The main goal of our laboratory is to understand the neurobiological basis for drug addiction. We use a multidisciplinary approach that incorporates behavioral pharmacology and molecular biology techniques to identify novel neuroadaptations produced by chronic drug exposure. Our research program is broadly divided into three areas of focus:

Our lab is interested in understanding the biological mechanisms underlying nicotine addiction. Drug self-administration is a clinically relevantanimal model that can be used to investigate the effects of potential smoking cessation medications in moderating nicotine reinforcement. Recent experiments aim to examine the role of acetylcholinesterase and nicotinic acetylcholine receptors in nicotine reinforcement and reinstatement.

Another focus of the laboratory is to integrate behavioral pharmacology and neuroscience with molecular techniques that probe drug-induced neuroadaptations at the genomic level. Specifically, our research aims to investigate the epigenetic mechanisms underlying drug craving and relapse. It is now clear that chronic exposure to drugs of abuse alters gene expression in limbic nuclei that underlies the neuronal and behavioral plasticity associated with drug taking and seeking. Our research is aimed at determining how drug-induced chromatin remodeling leads to alterations in growth factor expression following chronic cocaine.

Our previous studies have demonstrated that alterations in dopamine and glutamate transmission play a critical role in drug-taking and –seeking behaviors. Thus, one focus of our research program is to determine the molecular mechanisms that regulate plasticity in dopamine and glutamate systems and contribute to drug-seeking behavior. In collaboration with Dr. Chris Pierce, we are studying the role of protein kinase C (PKC) in cocaine priming-induced reinstatement, an animal model of relapse in human cocaine addicts. These studies also aim to understand how chronic cocaine exposure affects AMPA receptor trafficking in the nucleus accumbens.